Microbodies in experimentally altered cells. 8. Continuities between microbodies and their possible biologic significance.
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Biomedical subjects
Publications and source records attributed to D Svoboda.
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In an attempt to understand the nature of cytoplasmic and nuclear enlargement of liver cells designated as megalocytosis that results from chronic poisoning by lasiocarpine, a pyrrolizidine alkaloid, certain functional aspects of these cells were investigated together with the study of their morphology. The RNA polymerase activity of the megalocyte nuclei was essentially comparable to the activity observed in normal liver cells. Further, the inducibility of tryptophan pyrrolase activity by hydrocortisone, in the livers of rats treated chronically with lasiocarpine is an indication that translational mechanisms are intact. However, the increased uptake of 3H-thymidine by megalocytes, in the absence of observable mitotic activity, suggests that these cells are in the process of hypertrophy. It is concluded that the megalocytes are functionally normal cells, except that they are in the process of cellular hypertrophy and are incapable of division due to potent antimitotic action of the pyrrolizidine alkaloids.
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The liver cells of intact male rats given ethyl-alpha-p-chlorophenoxyisobutyrate (CPIB) characteristically show a marked increase in microbodies and in catalase activity, while those of intact female rats do not. In castrated males given estradiol benzoate and CPIB the increase in catalase activity and microbody proliferation is abolished, while in castrated females given testosterone propionate and CPIB the livers show a marked increase in microbodies and in catalase activity. No sex difference in microbody and catalase response is apparent in fetal and neonatal rats. Both sexes show a sharp rise in catalase activity on the day of birth, with a rapid decline at 5 days after birth. Thyroidectomy abolishes the hypolipidemic effect of CPIB in rats, but microbody proliferation and increase in catalase activity persists in thyroidectomized male rats, indicating that microbody proliferation can be independent of hypolipidemia. Adrenalectomy does not alter appreciably the microbody-catalase response to CPIB. These experiments demonstrate that (1) in adult rats, hepatic microbody proliferation is dependent to a significant degree upon male sex hormone but is largely independent of thyroid or adrenal gland hormones; (2) hepatic microbody proliferation is independent of the hypolipidemic effect of CPIB; (3) displacement of thyroxine from serum protein may not be sufficient cause for stimulation of microbody formation.
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